A 58-year-old woman with known cirrhosis from MASLD presents with 3 days of worsening confusion and abdominal distension. On exam: asterixis, ascites, temp 38.2°C, BP 92/60.
- Immediate priority: Diagnostic paracentesis — rule out SBP before assuming HE is the only problem. In patients with cirrhosis presenting with encephalopathy, SBP and HE can coexist.
- If ascitic fluid PMN ≥250 cells/mm³: start ceftriaxone + albumin immediately
- Assess for other HE precipitants: check BMP, CBC, blood cultures, urinalysis
- Start lactulose titrated to 2–3 soft bowel movements per day
- Check MELD 3.0 score — this presentation may represent a decompensation event that triggers transplant evaluation
Read through each section below to understand the pathophysiology, diagnosis, and management behind each step.
What Is Cirrhosis?
▼Cirrhosis is defined by diffuse hepatic fibrosis and nodule formation, disrupting normal liver architecture. It results from sustained hepatic injury across a range of etiologies: chronic viral hepatitis, alcohol-related liver disease, MASLD, autoimmune hepatitis, cholestatic diseases (PBC, PSC), and others.
Cirrhosis is broadly classified as compensated (no prior decompensation; 10-year survival ~80%) or decompensated (presence of ascites, variceal hemorrhage, hepatic encephalopathy, or jaundice; median survival ~2 years without transplantation).
Portal Hypertension: The Central Mechanism
▼Most complications of cirrhosis arise from portal hypertension — elevated pressure in the portal venous system due to increased vascular resistance from fibrosis and dynamic vasoconstriction. The hepatic venous pressure gradient (HVPG) is the gold standard measurement:
- HVPG ≥6 mmHg: portal hypertension
- HVPG ≥10 mmHg: clinically significant portal hypertension (CSPH) — risk of varices and decompensation
- HVPG ≥12 mmHg: risk of variceal hemorrhage
Ascites and Spontaneous Bacterial Peritonitis
▼Ascites is the most common complication of cirrhosis, occurring in ~50% of patients within 10 years of diagnosis. Pathophysiology: splanchnic vasodilation → decreased effective circulating volume → sodium and water retention.
Diagnosis: Serum-Ascites Albumin Gradient (SAAG) ≥1.1 g/dL confirms portal hypertension as the cause. See SAAG & Ascites → for the full workup.
Management: Sodium restriction (2 g/day), diuretics (spironolactone ± furosemide), large-volume paracentesis with albumin infusion for refractory cases, TIPS for refractory ascites.
Spontaneous Bacterial Peritonitis (SBP)
Life-threatening infection of ascitic fluid without an intra-abdominal source. Must be excluded in any patient with cirrhosis presenting with fever, abdominal pain, encephalopathy, or clinical deterioration.
Diagnosis: Ascitic fluid PMN count ≥250 cells/mm³. Treat empirically — do not wait for culture results.
Treatment: IV cefotaxime or ceftriaxone × 5 days + IV 25% albumin on day 1 and day 3 (reduces risk of hepatorenal syndrome).
Secondary prophylaxis: Norfloxacin is not available in the US; trimethoprim-sulfamethoxazole (TMP-SMX) or ciprofloxacin are used indefinitely after the first SBP episode.
↑ Back to topGastroesophageal Varices
▼Portosystemic collaterals that form when HVPG exceeds 10 mmHg. Variceal hemorrhage is the most immediately life-threatening complication of portal hypertension.
Primary prophylaxis: Non-selective beta-blockers (propranolol, carvedilol) or endoscopic variceal ligation (EVL) for medium/large varices.
Acute variceal hemorrhage management:
- Airway protection, resuscitation (restrictive transfusion strategy — target Hgb 7–8 g/dL)
- Vasoactive agents: octreotide IV for 3–5 days
- Antibiotics: ceftriaxone × 7 days (reduces infection and re-bleeding)
- Urgent upper endoscopy within 12 hours: EVL is preferred
- TIPS if endoscopic therapy fails
Hepatic Encephalopathy (HE)
▼Neuropsychiatric dysfunction caused by accumulation of neurotoxins (primarily ammonia) due to impaired hepatic detoxification and portosystemic shunting.
West Haven Grading: Grade 1 (mild confusion, sleep disturbance) → Grade 4 (coma). Covert HE (Grade 0–1) is common and under-recognized.
Precipitants (find and treat): infection/SBP, GI bleeding, dehydration, constipation, electrolyte disturbance, medications (benzodiazepines, narcotics), renal failure, dietary protein excess.
Treatment: Lactulose (targets colon pH and ammonia absorption), rifaximin (gut-selective antibiotic; reduces recurrence), identify and treat precipitants.
↑ Back to topHepatorenal Syndrome (HRS)
▼Functional renal failure in the setting of advanced liver disease and portal hypertension, in the absence of parenchymal kidney disease. Diagnosis of exclusion — first exclude hypovolemia and nephrotoxins.
- HRS-AKI (formerly type 1): Rapid progression. Median survival without treatment: weeks.
- HRS-CKD (formerly type 2): Slower progression, often associated with refractory ascites.
Treatment: Terlipressin (FDA-approved 2022) or norepinephrine + IV albumin. Liver transplantation is definitive therapy. See Hepatorenal Syndrome → for full management.
↑ Back to topHepatocellular Carcinoma (HCC) Surveillance
▼All patients with cirrhosis should undergo HCC surveillance with liver ultrasound ± AFP every 6 months. HCC is the most rapidly rising cause of cancer mortality in the US, and cirrhosis is present in ~80% of cases.
Early detection changes outcomes: transplant-eligible or resection-eligible HCC has excellent long-term survival. Late detection means palliative intent.
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